EGFR mutation and lobar location of lung adenocarcinoma

Chien Hua Tseng, Kun Chieh Chen, Kuo Hsuan Hsu, Jeng Sen Tseng, Chao Chi Ho, Te Chun Hsia, Kang Yi Su, Ming Fang Wu, Kuo Liang Chiu, Chien Ming Liu, Tzu Chin Wu, Hung Jen Chen, Hsuan Yu Chen, Chi Sheng Chang, Chung Ping Hsu, Jiun Yi Hsia, Cheng Yen Chuang, Chin Hung Lin, Jeremy J.W. Chen, Kuan Yu ChenWei Yu Liao, Jin Yuan Shih, Sung Liang Yu, Chong Jen Yu, Pan Chyr Yang, Tsung Ying Yang, Gee Chen Chang

研究成果: 雜誌貢獻文章同行評審

10 引文 斯高帕斯(Scopus)


The objective of this study was to investigate the associations among lung cancer location, and epidermal growth factor receptor (EGFR) mutation status. Treatment-naive, pathologically confirmed lung adenocarcinomas with tumor specimens available for genetic analysis were included from 2011 through 2014. Overall, 1771 patients with lung adenocarcinoma were included for analysis, after excluding those with carcinoma not otherwise specified, or synchronous multiple primary lung cancers. The median age was 64 years, and the female:male and never smoker:ever smoker ratios were 930:855 (52:48%) and 1167:604 (65:35%), respectively. The EGFR mutation rate was 56%. Among patients, 1093 (62%) had primary tumors in the upper lobes. Compared with the characteristics of the EGFR wild-type, tumors with EGFR activating mutations were more common in women (P < 0.001), never smokers (P < 0.001), and in the upper lobes (P = 0.004). Among EGFR activating mutations, compared with the EGFR exon 19 deletion, L858R mutation were more common in women (P = 0.002), never smokers (P = 0.038), and the upper lobes P < 0.0005). The present study is the first to address that different pulmonary lobar locations might harbor different EGFR mutation subtypes. We demonstrated that adenocarcinomas with L858R mutation, rather than exon 19 deletion or wild-type EGFR gene, prefer to locate over the upper lungs. This phenomenon was more significant in females and never-smokers, implying the result of complex interactions between genetic susceptibility and environmental factors. Therefore, EGFR L858R mutation and exon 19 deletion may not be identical disease entity from the point of carcinogenesis.

頁(從 - 到)157-162
出版狀態已發佈 - 9月 8 2015

ASJC Scopus subject areas

  • 癌症研究


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